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•  Ultraviolet (UV) radiation is classified into UVA, UVB, and UVC based on wavelengths ranging from 100 to 400 nm.

•  UVA (315-400 nm) accounts for 95% of UV radiation that is found in natural sunlight (1) and is subdivided into UVA2 (315-340 nm) and UVA1 (340-400 nm) (2).

•  UVA irradiation leads to formation of reactive oxygen species (ROS) (e.g. singlet oxygen), which results in oxidative stress (3).

•  In contrast to UVB, UVA is not completely filtered by clothing and penetrates into deep dermis, causing dermal damage (4-6).

•  Rodent studies have demonstrated that UVA is carcinogenic (7).

•  Sun protection factor (SPF) represents sunscreen efficacy to protect from erythema, which is mainly caused by UVB and UVA2, not UVA1.

INTRODUCTION

OBJECTIVES

Figure 1. UVA1 effect on thymidine dimer (A-F) and singlet oxygen production (G). (n = 3 per group, *p < 0.05, **p < 0.01, ***p < 0.001)

RESULTS (ex-vivo human skin)

Figure 3. UVA1 exposure and singlet oxygen production on volar forearm. (n = 6, *p < 0.05)

RESULTS (in-vivo human skin) MATERIALS AND METHODS

•  Exposure to UVA1 leads to singlet oxygen production and thymidine dimer formation.

•  Application of zinc oxide containing sunscreen and subsequent exposure to UVA1 light leads to a significant increase in singlet oxygen production.

•  Future directions: The role of antioxidants in

protection from UVA1 induced skin damage should be investigated.

CONCLUSIONS

REFERENCES

•  The primary aim of this study is to use a novel UVA1 emitting device to measure singlet oxygen production in real time.

•  The secondary aim is to measure singlet oxygen production after avobenzone and zinc oxide application and subsequent exposure to UVA1.

Suzana Bosanac, MAS*1; Waqas Burney, MBBS*2; Janice Leung3; Raja Sivamani, MD2 1 UC Davis School of Medicine; 2 Department of Dermatology, UC Davis; 3 University of California, Davis

UVA Light and Oxidative Stress

1. Schuch AP, Garcia CC, Makita K, and Menck CF. DNA damage as a biological sensor for environmental sunlight. Photochem Photobiol Sci. 2013;12(8):1259-72. 2. Marionnet C, Pierrard C, Golebiewski C, and Bernerd F. Diversity of biological effects induced by longwave UVA rays (UVA1) in reconstructed skin. PLoS ONE. 2014;9(8):e105263. 3. Panich U, Onkoksoong T, Limsaengurai S, Akarasereenont P, and Wongkajornsilp A. UVA-induced melanogenesis and modulation of glutathione redox system in different melanoma cell lines: the protective effect of gallic acid. Journal of photochemistry and photobiology B, Biology. 2012;108(16-22). 4. Menter JM, and Hatch KL. Clothing as solar radiation protection. Curr Probl Dermatol. 2003;31(50-63). 5. Sklar LR, Almutawa F, Lim HW, and Hamzavi I. Effects of ultraviolet radiation, visible light, and infrared radiation on erythema and pigmentation: a review. Photochem Photobiol Sci. 2013;12(1):54-64. 6. Wang F, Smith NR, Tran BA, Kang S, Voorhees JJ, and Fisher GJ. Dermal damage promoted by repeated low-level UV-A1 exposure despite tanning response in human skin. JAMA Dermatol. 2014;150(4):401-6. 7. de Laat A, van der Leun JC, and de Gruijl FR. Carcinogenesis induced by UVA (365-nm) radiation: the dose-time dependence of tumor formation in hairless mice. Carcinogenesis. 1997;18(5):1013-20.

Figure 2. Singlet oxygen production after sunscreen application and exposure to UVA1 (444.1mJ/cm2). (n = 3 per group, **p < 0.01)

Figure 4. Singlet oxygen production after sunscreen application to volar forearm and exposure to UVA1 (753.7 mJ/cm2). (n = 6, ***p < 0.001)

MATERIALS AND METHODS

Ex-vivo human skin: •  2cm2 exposed to no UVA1 (control), 26.5mJ/cm2, 171.2mJ/cm2,

444.1mJ/cm2 and 1091.2mJ/cm2 UVA1 à singlet oxygen measured à samples stained for thymidine dimer.

In-vivo human skin: •  The UC Davis IRB approved the in-vivo skin study. Written informed

consent was received from participants prior to inclusion in the study. •  2cm2 on volar forearms of healthy human subjects was measured and

exposed to 20.1mJ/cm2, 361.1mJ/cm2 or 735.7mJ/cm2 UVA1 à singlet oxygen production measured.